Some patients wth primary hypertension have sympathetic nerve dysfunction. We will attempt to determine whether the abnormality is a causative factor in their hypertension by correlating it with measurements of the cardiac index, peripheral vascular resistance, plasma and extra cellular volume, and the sodium/renin activity/aldosterone status. Decreased plasma volume may stimulate sympathetic tone. Conversely, increased plasma volume may inhibit sympathetic tone. Increased cardiac output, if occuring in some patients on a neurogenic basis, may be expected to be associated with a generalized increase in sympathetic tone. The latter has been associated with increased renin release and aldosterone excretion. We shall attempt to further define these relationships by investigating simultaneously three parameters: Catecholamine metabolism, cardiovascular measurements, and sodium/renin activity/aldosterone status in the individual patient. Candidates for study will be patients who have some evidence of sympathetic nerve dysfunction on the basis of increased plasma catecholamines, increased ratio of metanephrines to VMA, increase norepinephrine excretion, increased turnover rates of norepinephrine after dopa-3H, and clinical signs of sympathetic nerve hyperactivity. Comparitive studies will be made in hypertensive patients without sympathetic nerve dysfunction.